Loss of endothelial nitric oxide synthase exacerbates intestinal and lung injury in experimental necrotizing enterocolitis
Loss of endothelial nitric oxide synthase exacerbates intestinal and lung injury in experimental necrotizing enterocolitis
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DOI：
10.1016/j.jpedsurg.2018.02.087
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发表时间：
2018-06-01
影响因子：
2.4
通讯作者：
Markel, Troy A.
中科院分区：
文献类型：
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作者：
Drucker, Natalie A.;Jensen, Amanda R.;Markel, Troy A.
背景：坏死性小肠结肠炎（NEC）仍然是早产儿的一种毁灭性疾病。一氧化氮由内皮型一氧化氮合酶 (eNOS) 在肠道中合成，在肠系膜内充当有效的血管舒张剂和抗氧化剂，可能在预防 NEC 中发挥作用。我们假设，内皮一氧化氮的丧失会加重实验性 NEC 期间的肠道和相关肺损伤，并增加局部和全身炎症。方法：在 5 日龄的野生型 (WT) 和 eNOS 敲除 (eNOSKO) 幼鼠中诱导 NEC。实验组（n = 10）采用配方奶喂养并接受间歇性缺氧和低温应激，而对照组（n = 10）则继续与母亲一起进行母乳喂养。通过每日临床评估对幼崽进行监测。第九天处死后，评估肠和肺的损伤，并通过 ELISA 测量组织匀浆中的细胞因子。数据与 Mann-Whitney 进行比较，并 p
Background: Necrotizing enterocolitis (NEC) continues to be a devastating condition among preterm infants. Nitric oxide, which is synthesized in the intestine by endothelial nitric oxide synthase (eNOS), acts as a potent vasodilator and antioxidant within the mesentery and may play a role in prevention of NEC. We hypothesized that loss of endothelial nitric oxide would worsen both intestinal and associated lung injury and increase local and systemic inflammation during experimental NEC.Methods: NEC was induced in five-day-old wild type (WT) and eNOS-knockout (eNOSKO) mouse pups. Experimental groups (n = 10) were formula fed and subjected to intermittent hypoxic and hypothermic stress, while control groups (n = 10) remained with their mother to breastfeed. Pups were monitored by daily clinical assessment. After sacrifice on day nine, intestine and lung were assessed for injury, and cytokines were measured in tissue homogenates by ELISA. Data were compared with Mann-Whitney, and p